Respiratory Flashcards
4 most common drugs against TB
(Isoniazid) INH: primary drug used
rifampin
ethambutol
pyrazinamide
Isoniazid MOA
Suppresses bacterial growth by inhibiting synthesis of mycolic acid, a component of the mycobacterial cell wall.
Metabolized in the liver through acetylation—watch for “slow acetylators”
Isoniazid A/E and what to administer in high risk pt groups
Hepatotoxicity
Peripheral neuropathy
- Administer pyridoxine (Vitamin B6) daily in high risk groups (i.e., DM, ETOH abuse) or if patient develops neuropathy
Rifampin MOA
MOA: inhibits bacterial DNA-dependent RNA polymerase -> results in suppression of RN synthesis and protein synthesis
A/E of Rifampin
discoloration of bodily fluids
2 Analogs of Rifampin (close chemical make-up with same MOA and A/E)
Rifapentine
Rifabutin
Pyrazinamide (PZA) A/E
Non-gouty polyarthralgias – (pain in multiple joints)
Ethanbutol A/E
Optic neuritis – blurred vision, constriction of visual fields, & disturbance of color discrimination (red-green color blindness).
What is the most effective drug class for prevention / treatment of seasonal & perennial rhinitis - it reduces inflammation and edema
Intranasal Glucocorticoids (-sone)
Difference between H1 and H2 blockers (antihistamine)
H1 blockers are the drugs to which most people are referring when they use the term antihistamine. H1 blockers prevent the harmful effects of histamine and are used to treat seasonal allergic rhinitis, anaphylaxis, reactions to insect bites, and so forth.
H2 blockers are used to treat gastric acid disorders
When to take first generation antihistamines?
take at bedtime to avoid sedation
How to recognize first generation anti-histamine?
-amine
Common second generation anti-histamines?
Zyrtec, Claritin, Clarinex, Allegra
What is major difference between first and second generation anti-histamines?
Second generation poorly cross the blood-brain barrier; have a low affinity for H1 receptors in the CNS therefore does not cause sedation
Sympathomimetics (Decongestants) MOA
Reduce nasal congestion via activation of alpha1 adrenergic receptors on nasal blood vessels -> vasoconstriction
A/E to decongestants?
Rebound congestion (topicals) used for more than 5 days CNS stimulation (oral) – restlessness, anxiety, insomnia CV effects (oral) – tachycardia, inc. BP
Three classes of bronchodilators
beta2-adrenergic agonists
anticholinergics
xanthine derivatives
Give two categories of beta2 agonists and common drugs in each
Short Acting Beta Agonists: Albuterol
(think -buterol) Levalbuterol
Pirbuterol
Metaproterenol
Long acting beta agonist: Arformoterol
(think -moterol) Formoterol
Salmeterol
LABA are not used alone in management of asthma. What additional class is added to regime?
Inhaled Corticosteroids (-sone or -sonide)
Anticholinergics MOA
Acetylcholine (ACh) causes bronchial constriction and narrowing of the airways.
Anticholinergics bind to the ACh receptors, preventing ACh from binding.
Result: bronchoconstriction is prevented, airways dilate
Xanthines MOA
Action: inhibits phophodiesterase, an enzyme responsible for breaking down cAMP. Because this enzyme is inhibited, more cAMP is available for bronchodilation.
Common Xanthine drugs (THEO-DUR)
Theophylline / iv form - aminophylline
First and late sign of toxicity in patients receiving xanthine drug
Early - Nausea
Late - Tremors, Dysrhythmia and Convulsions
Leukotriene Receptor Antagonist MOA
Leukotrienes are substances released when a trigger, such as cat hair or dust, starts a series of chemical reactions in the body.
Leukotrienes cause inflammation, bronchoconstriction, and mucus production
By blocking those receptors, you block that cascade
Leukotriene receptor antagonist suffix
-kast
Mast Cell Stabilizers MOA
Stabilize mast cells, reducing the release of mast cell chemicals that cause bronchoconstriction, edema, and inflammation. Interrupts migration of eosinophils into site
Common Mast Cell Stabilizer drug
Cromolyn
Inhaled Corticosteroids (ICS) MOA
Work by suppressing inflammation
Decrease synthesis & release of inflammatory mediators including leukotrienes, histamine, prostaglandins
Decrease infiltration & activity of inflammatory cells including eosinophils, leukocytes
Decrease edema of the airway mucosa 2nd to a decrease in vascular permeability
A/E of the -sone or -sonide drugs (ICS)
Oropharyngeal candidiasis
Dysphonia (hoarseness)
Step-wise approach to asthma control
Step 1 Short-acting inhaled beta2 agonist as needed
Step 2 Preferred: low-dose inhaled corticosteroid (ICS).
-Alternative: cromolyn, nedocromil, leukotriene receptor antagonist (LTRA), or theophylline
Step 3 Low-dose ICS and long-acting beta2 agonist (LABA) or medium-dose ICS
-Alternative: low-dose ICS and either LTRA, theophylline, or zileuton
Step 4 Preferred: medium-dose ICS plus LABA
-Alternative: medium-dose ICS plus either LTRA, theophylline, or zileuton
Step 5 High-dose ICS and LABA, and consider omalizumab for patients with allergies
Step 6 High-dose ICS and LABA and oral corticosteroid, and consider omalizumab for patients with allergies
Anticholinergic Agents (how to recognize) and contraindicated in which patient population
-tropium bromide / may increase intraocular pressure - glaucoma pt’s
Expectorants MOA and common drug
remove viscid (sticky) secretions by reduction of the adhesiveness & surface tension. Guaifenesin (aka musinex and robitussin)
Antitussive MOA
Suppresses the cough reflex in the medulla
Common opioid antitussive
Common non-opioid antitusive
Codeine
Dextromethorphan and Benzonatate
Acetylcysteine is common drug found in which class; MOA
Mucolytic Agents; Action – works directly on mucus to reduce thickness & make secretions less tenacious.
What drug is indicated for patient with acetaminophen overdose?
Acetylcysteine
Pulmonary arterial hypertension pathophysiology
Pulmonary hypertension is a type of high blood pressure that affects the arteries in the lungs and the right side of the heart.
Pulmonary hypertension begins when tiny arteries in lungs, called pulmonary arteries, and capillaries become narrowed, blocked or destroyed. This makes it harder for blood to flow through the lungs, and raises pressure within the lungs’ arteries. As the pressure builds, your heart’s lower right chamber (right ventricle) must work harder to pump blood through your lungs, eventually causing your heart muscle to weaken and eventually fail.
3 drug classes indicated for pulmonary hypertension
Prostacyclin Analogs
Endothelian 1 receptor antagonist
Phosphodiesterase Type 5 Inhibitors (-afil)
Lung surfactant: Porcine extract of lung surfactant given to neonates w/ respiratory distress syndrome (how to recognize drug)
-actant
